chapter 42 Flashcards
What is Gastroesophageal Reflux Disease (GERD)?
GERD is considered pathologic gastroesophageal reflux (GER) that occurs when the passage of gastric contents into the esophagus induces troublesome symptoms or complications (such as esophagitis or structuring) that affect daily functioning. This is different from normal, nonpathologic GER, which is common in healthy infants and children.
What are the key factors in the pathophysiology of GERD?
GERD is influenced by genetic, environmental, anatomic, hormonal, and neurogenic factors. The most common cause is transient lower esophageal sphincter relaxations (TLESRs). Inadequate adaptation of sphincter tone to changes in abdominal pressure can also be implicated. Factors maintaining lower esophageal sphincter integrity include the location of the gastroesophageal junction in a high-pressure zone, mucosal gathering within the sphincter, and the angle of the esophagus entering the stomach. Other mediators include esophageal peristalsis or clearance, mucosal resistance, and delayed gastric emptying. Reflux of acidic gastric contents leads to inflammation of the esophageal epithelium (esophagitis) and stimulation of the vomiting reflex.
How does GERD typically present in infants?
nfants with GERD may present with:
◦Irritability
◦Sleep disturbance
◦Excessive regurgitation
◦Hematemesis
◦Unexplained crying
◦Back arching
◦Food refusal or anorexia
◦Failure to thrive (FTT)
How does GERD typically present in older children and adolescents?
Older children and adolescents may present with:
◦Decreased food intake
◦Weight loss
◦Abdominal or epigastric pain
◦Symptoms similar to adults, such as heartburn and regurgitation.
What are potential complications of GERD?
◦Esophageal complications: Esophagitis, hemorrhage, stricture, Barrett esophagus, and rarely, adenocarcinoma.
◦Extraesophageal symptoms: Cough, wheezing, stridor, laryngitis, pharyngitis, dental erosions, sinusitis, recurrent otitis media, and Sandifer syndrome.
How is GERD evaluated?
Evaluation: Clinical manifestations are often adequate for diagnosis. Barium contrast studies may rule out anatomical abnormalities but are not recommended for GERD diagnosis. pH metry can correlate troublesome symptoms and assess acid suppression therapy efficacy
How is GERD treated?
Treatment:
▪Breast-fed babies: Maternal elimination of cow’s milk protein may be recommended.
▪Formula-fed infants: Feeding volume and frequency adjustments using extensively hydrolyzed protein or amino acid–based formulas may be needed.
▪Thickened feedings are recommended for visible regurgitation and/or vomiting in infants.
▪Lifestyle changes for children and adolescents include weight loss, smoking cessation, sleeping position changes, and avoiding caffeine, chocolate, alcohol, and spicy foods.
▪Medications to buffer or reduce gastric acid secretion, increase motility, or increase lower esophageal sphincter pressure may be used.
▪Surgical intervention (anti-reflux procedure, including gastropexy and fundoplication) is considered if medical management fails or the child has life-threatening reflux events.
What is diarrhea and what are the general pathophysiologic mechanisms?
Diarrhea is an increase in the water content, volume, or frequency of stools, usually defined as three or more watery or loose stools in 24 hours. Diarrhea lasting longer than 4 weeks is considered chronic. The pathophysiologic mechanisms include:
◦Increased fluid secretion into the GI lumen (secretory diarrhea).
◦Drawing fluid into the lumen by osmosis (osmotic diarrhea).
◦Reduced intestinal transit time with luminal fluid retention (intestinal dysmotility).
◦Inflammation resulting in malabsorption and increased luminal osmotic load (inflammatory diarrhea).
What are common causes of diarrhea in infants and children?
Common causes include:
◦Viral, bacterial, and systemic infections.
◦Malabsorption syndromes.
◦Autoimmune disorders.
◦Congenital malformations.
◦Genetic disorders.
◦Acute infection (most common cause worldwide).
◦Association with the COVID-19 pandemic.
◦Antibiotic therapy.
◦Appendicitis.
◦Chemotherapy.
◦Inflammatory bowel disease (IBD).
◦Parasitic infestation.
◦Parenteral infections.
◦Ingestion of toxic substances.
What are common viral and bacterial agents causing acute infectious diarrhea?
Viruses: Rotaviruses (most common in young children), noroviruses, and adenoviruses.
◦Bacteria: Various bacteria depending on geographic location. Clostridium difficile is often associated with previous antibiotic therapy
How does acute infectious diarrhea present and what are potential complications?
Clinical Manifestations: Rapid onset, watery stools (sometimes with blood), abdominal cramping, fever, vomiting, and weight loss.
◦Complications: Severe dehydration, acidosis, and shock can occur quickly. Hemolytic uremic syndrome and renal failure can develop with Shigella toxin and Escherichia coli infection.
How is acute infectious diarrhea evaluated ?
History, stool testing for common pathogens, and laboratory analysis
How is acute infectious diarrhea treated?
Treatment: Hydration, electrolyte replacement, nutrition maintenance, and antibiotics if a pathogen is found. Antispasmodics may relieve cramping, and selected probiotics may reduce duration and improve outcomes. Intravenous solutions are used if oral solutions are not tolerated. Prevention includes clean water, sanitation, and good hygiene.
What is primary lactose intolerance?
Primary lactose intolerance is an acquired deficiency of lactase, rarely manifesting before age 5, leading to the small bowel’s inability to absorb ingested lactose (lactose malabsorption) and subsequent clinical symptoms upon lactose consumption.
What is the pathophysiology and what are the symptoms of primary lactose intolerance?
Malabsorption of lactose leads to osmotic diarrhea accompanied by abdominal pain, diarrhea, and flatulence.
How is primary lactose intolerance diagnosed?
Elimination of dietary lactose, hydrogen lactose breath test, or oral lactose tolerance test
How is primary lactose intolerance treatment?
Reducing milk consumption or supplementing with oral lactase. Tolerance may be improved with fermented dairy products or soy food. A low-FODMAP diet or probiotics may help with persistent symptoms. Consider additional dietary calcium and vitamin D
What is neonatal jaundice and what are the two main categories?
Neonatal jaundice (icterus) is a yellow pigmentation of the skin, mucus membranes, or eyes caused by an increased level of bilirubin in the bloodstream. The two main categories are:
◦Physiologic jaundice (hyperbilirubinemia): Common in healthy newborns due to immature bilirubin uptake and conjugation. Poor caloric intake or dehydration can contribute.
◦Pathologic jaundice: Appears within 24 hours after birth, with higher bilirubin concentrations, association with severe illness, or a rapid rise in bilirubin levels.
What are common causes of pathologic jaundice?
Causes include:
◦Increased bilirubin production (e.g., hemolysis due to blood group incompatibility).
◦Impaired hepatic uptake or excretion of unconjugated bilirubin.
◦Delayed maturation of liver bilirubin conjugating mechanisms.
◦Hemolytic disease of the newborn (erythroblastosis fetalis).
◦Metabolic and endocrine disorders.
◦Anatomic abnormalities of the liver.
◦Infections.
◦Risk factors such as prematurity, maternal diabetes, and delayed meconium passage.
How can high bilirubin levels be harmful in newborns?
Unconjugated bilirubin is lipid soluble and can cross the blood-brain barrier in infants. Bilirubin encephalopathy (kernicterus) is caused by the deposition of toxic, unconjugated bilirubin in brain cells.
What are the clinical manifestations of neonatal jaundice?
Physiologic jaundice: Develops on the second or third day after birth and subsides within 1-2 weeks in full-term infants and 2-4 weeks in premature infants.
◦Pathologic hyperbilirubinemia: Increasing bilirubin values and persistent jaundice beyond the typical timeframe. Manifestations include yellowing of the skin, dark urine, light-colored stools, and weight loss. Premature infants with respiratory distress, acidosis, or sepsis are at higher risk for kernicterus and bilirubin-induced neurologic dysfunction (BIND).
How is neonatal jaundice evaluated?
Evaluation: Clinical assessment, monitoring of total and direct (conjugated) bilirubin levels, and evaluation of the bilirubin/albumin ratio. Other causes of jaundice must be ruled out for physiologic jaundice.
How is neonatal jaundice treated?
Treatment:
▪Physiologic jaundice: Commonly treated with phototherapy.
▪Pathologic jaundice: May require exchange transfusion and treatment of the underlying disorder.
What is hepatitis?
Hepatitis refers to inflammation of the liver. It can be self-limiting or lead to cirrhosis, liver cancer, and death. Etiologies include toxic substances, viral infections, other infections, and autoimmune diseases. There are five main types of viral hepatitis.
How is Hepatitis A transmitted, and what are its characteristics?
Transmission: Fecal-oral route.
◦Incubation period: 28 days.
◦Often asymptomatic in children younger than 6 years. Older children and adults typically present with symptoms.
◦Replicates in the liver and is excreted in stool. Viral shedding is highest in the 2 weeks before symptom onset. Children can shed longer than adults.
◦Outbreaks can occur in day-care centers, households, and through contaminated food or water.
◦Symptoms, if present, are mild and may include nausea, vomiting, and diarrhea. Jaundice is more likely in older children.
◦Almost all children recover without residual liver damage. Immunity develops after infection. Vaccination is effective in reducing incidence.
How is Hepatitis B transmitted, and what are its potential outcomes?
Transmission: Contact with infected blood and body fluids. Risk factors include infected mothers, household contacts, parenteral drug abuse, and unprotected sex. Vertical and horizontal early childhood transmission are main routes for children.
◦Chronic hepatitis may develop more often in young children due to immature immune systems. Cirrhosis and hepatocellular carcinoma are rare in childhood. Fulminant hepatitis occurs in 1% of cases and may be increased with co-infection.
◦Vaccination programs have reduced incidence. Immunoprophylaxis and vaccination at birth are recommended to prevent perinatal transmission. Treatment is conservative, with antivirals for chronic disease.
How is Hepatitis C transmitted in children, and what is its course?
Transmission in children: Most commonly vertical (mother-to-child), enhanced by maternal HIV co-infection. In older children, through infected blood or materials and sexual encounters. Transmission from blood transfusions is now negligible.
◦Spontaneous resolution is high with vertical transmission; otherwise, the disease is usually mild in children, and cirrhosis is rare. Treatment is genotype-specific, with antiviral drugs used in children with persistently elevated liver enzymes or progressive liver disease. Cure is infrequent with current treatments.
What are the characteristics of Hepatitis D Virus?
HDV is a single-strand RNA virus that requires HBV for replication. Infection occurs simultaneously with HBV or as a superinfection. Vertical transmission is uncommon. Prevalence in the US is low but affects parts of Europe and Asia, causing progressive liver disease in chronic HBV carriers. Treatment is based on genotype, and research for novel treatments is ongoing
What are the main causes and manifestations of chronic hepatitis in children?
Main causes: HBV and HCV.
Manifestations: May include malaise, anorexia, fever, GI bleeding, hepatomegaly, edema, and transient joint pain, but often there are no symptoms. Elevated serum alanine aminotransferase and bilirubin levels may be present. Evidence of impaired liver synthetic function (prolonged prothrombin time, thrombocytopenia, hypoalbuminemia) may occur. Diagnosis is based on clinical manifestations and liver biopsy.
How is chronic hepatitis treated, and what is the potential outcome?
There is no curative therapy for chronic HBV or HCV. Children are treated with antiviral drugs and require ongoing monitoring. Liver transplantation may eventually be necessary. Autoimmune hepatitis (AIH) or autoimmune primary sclerosing cholangitis (PSC) are other forms with unknown etiology, thought to be immunologic, environmental, or genetic. PSC is associated with IBD. These are chronic and progressive diseases
What is cirrhosis and what are its complications in children?
Cirrhosis is fibrotic scarring of the liver in response to inflammation and tissue damage, resulting in nodular obstruction to blood and bile flow. Most forms of chronic liver disease in children can rarely progress to cirrhosis. Complications in children are similar to adults: portal hypertension, collateral vessel formation, and varices. Children with cirrhosis also experience growth failure due to nutritional deficits and developmental delay, particularly in gross motor function due to ascites and weakness. The cause of cirrhosis can influence its severity. Early identification and treatment of the underlying cause may stabilize some types.
What is Nonalcoholic Fatty Liver Disease (NAFLD)?
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in children. It is associated with obesity, insulin resistance, genetic predisposition, ethnicity, gut microbiome, and environmental factors (diet and lack of exercise). NAFLD can progress to cirrhosis and cardiometabolic syndrome if untreated. Diagnosis is made by excluding other causes, usually by age 12-13. Liver biopsy is needed for definitive diagnosis of nonalcoholic steatohepatitis (NASH). Treatment focuses on exercise, weight loss with a low glycemic index diet. Pharmacologic agents are being evaluated.
